How Hydrogen Gas Protects Against Inflammation and Brain Injury

Authors
Journal
Current Pharmaceutical Design
Year
DOI
10.2174/1381612826666200925123510
Study Type
clinical
Peer Reviewed
Yes
Country
Japan
Health Condition
Inflammatory Diseases
Body System
Nervous System

TL;DR

Scientists discovered that breathing in hydrogen gas can help protect your body from inflammation and injury, not just by cleaning up harmful molecules like we thought, but also by triggering your cells' natural defense systems to get stronger and tougher against damage. This could lead to new treatments for diseases caused by inflammation and injuries.

Key Finding

Hydrogen gas appears to protect against inflammatory diseases and ischemic injury through multiple mechanisms beyond simple free radical scavenging, including triggering a cellular stress response called mitohormesis that activates protective pathways like Nrf2.

Summary

This review examines how hydrogen gas (H2) may protect the body against inflammatory diseases and injury from reduced blood flow to the brain. While hydrogen was long thought to be inactive in the human body, recent research shows it can reduce harmful molecules called free radicals and trigger protective stress responses in cells. The authors suggest that hydrogen's benefits come from multiple mechanisms working together, including activating a cellular defense pathway called Nrf2 and regulating the immune system, rather than just acting as a simple antioxidant.

Practical Takeaway

This is a review article summarizing existing research rather than a new study, and it does not include human trials. While it suggests hydrogen may have therapeutic potential through multiple biological pathways, the authors note that more research is needed to understand exactly how hydrogen works in the body and to develop effective medical applications. Anyone considering hydrogen water should be aware that most evidence to date comes from laboratory and animal studies.

Abstract

Because multicellular organisms do not have hydrogenase, H2 has been considered to be biologically inactive in these species, and enterobacteria to be largely responsible for the oxidation of H2 taken into the body. However, we showed previously that inhalation of H2 markedly suppresses brain injury induced by focal ischemia-reperfusion by buffering oxidative stress. Although the reaction constant of H2 with hydroxyl radical in aqueous solution is two to three orders of magnitude lower than that of conventional antioxidants, we showed that hydroxyl radical generated by the Fenton reaction reacts with H2 at room temperature without a catalyst. Suppression of hydroxyl radical by H2 has been applied in ophthalmic surgery. However, many of the anti-inflammatory and other therapeutic effects of H2 cannot be completely explained by its ability to scavenge reactive oxygen species. H2 administration is protective in several disease models, and preculture in the presence of H2 suppresses oxidative stress-induced cell death. Specifically, H2 administration induces mitochondrial oxidative stress and activates Nrf2; this phenomenon, in which mild mitochondrial stress leaves the cell less susceptible to subsequent perturbations, is called mitohormesis. Based on these findings, we conclude that crosstalk between antioxidative stress pathways and the anti-inflammatory response is the most important molecular mechanism involved in the protective function of H2 , and that regulation of the immune system underlies H2 efficacy. For further medical applications of H2 , it will be necessary to identify the biomolecule on which H2 first acts.